Global analysis of protein-RNA interactions in SARS-CoV-2 infected cells reveals key regulators of infection
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ABSTRACT:
PROVIDER: PRJNA719366 | ENA |
REPOSITORIES: ENA
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Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19. SARS-CoV-2 relies on cellular RNA-binding proteins (RBPs) to replicate and spread, although which RBPs control SARS-CoV-2 infection remains largely unknown. Here, we employ a multi-omic approach to identify systematically and comprehensively which cellular and viral RBPs are involved in SARS-CoV-2 infection. We reveal that the cellular RNA-bound proteome is remodelled upon SARS-CoV-2 infection, having widespread effects on RNA metabolic pathways, non-canonical RBPs and antiviral factors. Moreover, we apply a new method to identify the proteins that directly interact with viral RNA, uncovering dozens of cellular RBPs and six viral proteins. Amongst them, several components of the tRNA ligase complex, which we show regulate SARS-CoV-2 infection. Furthermore, we discover that available drugs targeting host RBPs that interact with SARS-CoV-2 RNA inhibit infection. Collectively, our results uncover a new universe of host-virus interactions with potential for new antiviral therapies against COVID-19.
2021-05-29 | GSE171382 | GEO
Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19. SARS-CoV-2 relies on cellular RNA-binding proteins (RBPs) to replicate and spread, although which RBPs control SARS-CoV-2 infection remains largely unknown. Here, we employ a multi-omic approach to identify systematically and comprehensively the cellular and viral RBPs that are involved in SARS-CoV-2 infection. We reveal that SARS-CoV-2 infection profoundly remodels the cellular RNA-bound proteome, which includes wide-ranging effects on RNA metabolic pathways, non-canonical RBPs and antiviral factors. Moreover, we apply a new method to identify the proteins that directly interact with viral RNA, uncovering dozens of cellular RBPs and six viral proteins. Amongst them, several components of the tRNA ligase complex, which we show regulate SARS-CoV-2 infection. Furthermore, we discover that available drugs targeting host RBPs that interact with SARS-CoV-2 RNA inhibit infection. Collectively, our results uncover a new universe of host-virus interactions with potential for new antiviral therapies against COVID-19.
2021-09-09 | PXD023418 | Pride
Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19). SARS-CoV-2 relies on cellular RNA-binding proteins (RBPs) to replicate and spread, although which RBPs control its life cycle remains largely unknown. Here, we employ a multi-omic approach to identify systematically and comprehensively the cellular and viral RBPs that are involved in SARS-CoV-2 infection. We reveal that SARS-CoV-2 infection profoundly remodels the cellular RNA-bound proteome, which includes wide-ranging effects on RNA metabolic pathways, non-canonical RBPs, and antiviral factors. Moreover, we apply a new method to identify the proteins that directly interact with viral RNA, uncovering dozens of cellular RBPs and six viral proteins. Among them are several components of the tRNA ligase complex, which we show regulate SARS-CoV-2 infection. Furthermore, we discover that available drugs targeting host RBPs that interact with SARS-CoV-2 RNA inhibit infection. Collectively, our results uncover a new universe of host-virus interactions with potential for new antiviral therapies against COVID-19.
| S-EPMC8142890 | biostudies-literature
Project description:For the assessment of host response dynamics to SARS-CoV and SARS-CoV-2 infections in human airway epithelial cells at ambient temperature corresponding to the upper or lower respiratory tract. We performed a temporal transcriptome analysis on human airway epithelial cell (hAEC) cultures infected with SARS-CoV and SARS-CoV-2, as well as uninfected hAEC cultures, incubated either at 33°C or 37°C. hAEC cultures were harvested at 24, 48 72, 96 hpi and processed for Bulk RNA Barcoding and sequencing (BRB-seq), which allows a rapid and sensitive genome-wide transcriptomic analysis in a highly multiplexed manner. Transcriptome data was obtained from a total of 7 biological donors for pairwise comparisons of SARS-CoV or SARS-CoV-2 virus-infected to unexposed hAEC cultures at respective time points and temperatures.
2020-11-27 | E-MTAB-9781 | biostudies-arrayexpress
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2013-05-28 | E-GEOD-11704 | biostudies-arrayexpress
Project description:The pandemic of the novel Coronavirus SARS-CoV-2, cause of Covid-19, has caused tens of thousands of deaths since its emergence in late 2019. An in-depth knowledge of the molecular biology of the virus infection is key for a better understanding of the virus and the progression of the disease. We here provide analysis of changes in proteome and phosphoproteome of H1299 cells untreated or treated with SARS-CoV or SARS-CoV-2 on a time course (4, 12, 24, 36 hrs).
2020-04-24 | PXD018581 | Pride
Project description:Bulk RNA sequencing was performed on control and SARS-CoV and SARS-CoV-2 infected intestinal organoids.
2020-05-01 | GSE149312 | GEO
Project description:We performed RNAseq analysis on primary human airway epithelial cultures either mock infected (PBS) or infected with SARS-CoV-2. Transcriptional profiling studies found that infected pHAE cells had a molecular signature dominated by pro-inflammatory cytokines and chemokine induction, including IL-6, TNFα, CXCL8, and identified NF-κB and ATF4 as key drivers of this pro-inflammatory cytokine response. Surprisingly, we observed a lack of a type I or III interferon (IFN) response to SARS-CoV-2 infection
2020-07-21 | GSE153970 | GEO
Project description:Purpose: The goal of this study is to define the transcriptional response of H522 cells to SARS-CoV-2 infection. Methods:H522 cells were infected with SARS-CoV-2 at varying multiplicities of infection and samples processed for RNA-seq at 4, 24, 48, 72 and 96 hours post-infection. Results: We provide the transcriptomic and translatomic landscape of SARS-CoV-2-infected H522 cells from multiple RNA-seq libraries. We found that the robust transcriptional upregulation of numerous type I interferon and cell cycle associated genes in SARS-CoV-2-infected cells. Conclusions: Our study represents the detailed analysis of transcriptional responses of H522 cells to SARS-CoV-2 and demonstrates upregulation of key pathways that may paly a role in disease pathogenesis.
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| 12454 | ecrin-mdr-crc